Two-thirds of all breast cancers display mutations in the tumor suppressor p53 (Lai et al. (2004) Breast Cancer Res. Treat., 83: 57-66), and one-third of all advanced human breast carcinomas demonstrate a marked reduction in expression of the pro-apoptotic Bcl-2 family member Bax (Krajewski et al. (1995) Cancer Res., 55: 4471-4478). Bax and p53 mutations are associated with a high percentage of all human tumors. The subgroup of patients displaying p53 mutations or reduced Bax expression generally respond poorly to therapy and exhibit rapidly growing tumors and shorter median survival (Lai et al., supra; Reed (1996) J. Clin. Invest., 97:2403-2404). Though extensively pursued, the mechanism by which Bax expression is regulated in normal, malignant, or dying cells is unknown. The only known endogenous activator of Bax expression is the p53 transcription factor, which is responsible for inducing cell death in cancerous and damaged cells (Miyashita and Reed (1995) Cell, 80: 293-299).